Proteome analysis reveals translational inhibition of Caenorhabditis elegans enhances susceptibility to Pseudomonas aeruginosa PAO1 pathogenesis

2016 ◽  
Vol 145 ◽  
pp. 141-152 ◽  
Author(s):  
Vigneshkumar Balasubramanian ◽  
Durai Sellegounder ◽  
Kundu Suman ◽  
Balamurugan Krishnaswamy
Keyword(s):  
Pseudomonas Aeruginosa ◽  
Caenorhabditis Elegans ◽  
Proteome Analysis ◽  
Pseudomonas Aeruginosa Pao1 ◽  
Translational Inhibition

scholarly journals Red death in Caenorhabditis elegans caused by Pseudomonas aeruginosa PAO1

2009 ◽  
Vol 106 (15) ◽  
pp. 6327-6332 ◽  
Author(s):  
A. Zaborin ◽  
K. Romanowski ◽  
S. Gerdes ◽  
C. Holbrook ◽  
F. Lepine ◽  
...  
Keyword(s):  
Pseudomonas Aeruginosa ◽  
Caenorhabditis Elegans ◽  
Pseudomonas Aeruginosa Pao1

scholarly journals Pseudomonas aeruginosa cleaves the decoding center of Caenorhabditis elegans ribosomes

PLoS Biology ◽  
2020 ◽  
Vol 18 (12) ◽  
pp. e3000969
Author(s):  
Alejandro Vasquez-Rifo ◽  
Emiliano P. Ricci ◽  
Victor Ambros
Keyword(s):  
Pseudomonas Aeruginosa ◽  
Caenorhabditis Elegans ◽  
Ribosomal Rna ◽  
Genomic Analysis ◽  
Host Protein ◽  
Dependent Manner ◽  
Exotoxin A ◽  
Helix 69 ◽  
Translational Inhibition ◽  
Host Protein Synthesis

Pathogens such as Pseudomonas aeruginosa advantageously modify animal host physiology, for example, by inhibiting host protein synthesis. Translational inhibition of insects and mammalian hosts by P. aeruginosa utilizes the well-known exotoxin A effector. However, for the infection of Caenorhabditis elegans by P. aeruginosa, the precise pathways and mechanism(s) of translational inhibition are not well understood. We found that upon exposure to P. aeruginosa PA14, C. elegans undergoes a rapid loss of intact ribosomes accompanied by the accumulation of ribosomes cleaved at helix 69 (H69) of the 26S ribosomal RNA (rRNA), a key part of ribosome decoding center. H69 cleavage is elicited by certain virulent P. aeruginosa isolates in a quorum sensing (QS)–dependent manner and independently of exotoxin A–mediated translational repression. H69 cleavage is antagonized by the 3 major host defense pathways defined by the pmk-1, fshr-1, and zip-2 genes. The level of H69 cleavage increases with the bacterial exposure time, and it is predominantly localized in the worm’s intestinal tissue. Genetic and genomic analysis suggests that H69 cleavage leads to the activation of the worm’s zip-2-mediated defense response pathway, consistent with translational inhibition. Taken together, our observations suggest that P. aeruginosa deploys a virulence mechanism to induce ribosome degradation and H69 cleavage of host ribosomes. In this manner, P. aeruginosa would impair host translation and block antibacterial responses.

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